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About 75% of its consumption is used in
production of steel and alloys.

It is used :

- in the production of very resistant
alloys. One employs the alloy aluminium-nickel-cobalt for the
manufacture of magnets;

-in the industry of hard metal or
fritted metals. The cobalt-carbide of tungsten mixture is
particularly resistant (hardness from 90% to 95% of that of
diamond). It is used to manufacture teeth of saws, drilling
machines, drills, bits for drills;

- in the ceramic and glass industry
cobalt salts are used for the preparation of glazes and colouring
materials;

-in cobalt plating of metals by
electrolysis, it covers them with a shiny finish more resistant
than nickel;

-in the body of certain tools as a union
material with their tungsten ends.

The grinding of surgical and dental
prostheses (alloy with nickel, chromium and molybdenum) can
involve exposure to cobalt as well as the polishing of diamonds
using discs made up of microdiamonds whose binding agent is
cobalt.

Animals given cobalt chloride perorally
or via injections show higher concentrations in the liver, with
somewhat lower concentrations in the kidney and spleen.

Cobalt salts inhalation causes
respiratory irritation possibly leading to pulmonary oedema
(chemical pneumonia) in animals. Inhalation studies in hamsters
did not show any increase in tumors from cobalt oxide.

Its polycythemic action resembles the
human essential variety. This action would result from its
in vivo unstable action on renal lysosomes causing the
secretion of a factor stimulating the production of
erythropoetin.

Pancreatic lesions have been observed in
animals but, the pancreatic cells effects are reversible by
hyperglycemia.

Cobalt may cause myocardial
degeneration.

Cancers (lung cancer,
rhabdomyofibrosarcoma) may be caused in animals, at least when
cobalt (oxide dust, chloride) is administered parenterally or
intratracheally.

In procaryotic cells in vitro,
divalent cobalt compounds (CoII) do not cause any mutagenic
action.

Cobalt chloride in vivo, does
not seem to be foetotoxic nor teratogenic in the rat; but at high
doses, it may cause testicular degeneration in rodents which is
partly reversible with the administration of zinc.

For the general population, food and
beverages represent the main source of cobalt exposure. Traces of
cobalt are also present in various household products.

One atom of cobalt comprises the central
and necessary core in the vitamin B12, or cyanocobalamin, molecule
which is an essential vitamin.

Its deficiency may cause anemia.

Polycythemia has been reported in heavy
drinkers of cobalt fortified beer.

Cobalt per se is not essential for
humans or other mammals.

II-Routes of Absorption and Exposure
:

The usual routes of absorption are
ingestion and inhalation.

Absorption through the skin can occur
for certain compounds but is low.

The main source of absorption during
occupational exposure is via the respiratory tract.

III-Biochemokinetics :

Cobalt is not a cumulative toxin.

The normal daily intake by ingestion is
estimated at 20-40µg.

The total body burden is about 1.5
mg.

After absorption, cobalt is mainly
distributed to the liver.

Cobalt is mainly excreted in urine and
to a lesser extent via faeces.

Gastrointestinal absorption of
radioactive cobalt chloride in humans has been estimated to be
about 18%. Eight days after parenteral administration, 56% and 11%
of the given dose is eliminated via urine and feces,
respectively.

Following initial rapid elimination, the
remaining 10% usually clears slowly with a biologic half-time of
about 2 years.

Relatively high concentrations are also
found in the myocardium (heart).

The major proportion of parenterally
administered cobalt is rapidly cleared from the body, mainly via
the urine.

Cobalt concentrations of 90µg/m3 in
air have been reported to give cobalt concentration of about
100µg/L urine after a work shift, decreasing to less than
half this concentration within 1 day.

The normal concentrations of cobalt in
blood and urine from non-occupationally exposed persons are about
0.1 to 2µg/L. The levels of cobalt in blood, and particularly
in urine, increase in proportion to the level of occupational
exposure and may be used for biologic monitoring in order to
assess individual exposure.

Elimination of cobalt is considerably
slower in uremic patients.

IV-Symptoms and Signs :

A-Acute Toxicity :

Possible irritation of :

-skin;

-eyes;

-respiratory tract

If ingested or inhaled in large amounts
:

-nausea;

-vomiting;

-diarrhoea;

-epigastric pain.

B-Chronic Toxicity

1-Non-Occupational Intoxication
:

Endemic outbreaks of cardiomyopathy with
mortality rates up to 50% have been described among heavy
consumers (up to 10L/day) of cobalt-contaminated beer giving an
exposure of a few milligrams per day.

It has been suggested that the
cardiomyopathy had a multicausal origin, since cobalt exposure
from beer was considerably lower than the doses prescribed to
patients with anemia.

Other factors of importance are high
alcool intake combined with a generally poor nutritional
status.

This practice of fortifying beer with
cobalt chloride in order to improve the stability of the foam has
now been abandoned.

Shortness of breath, pharyngeal
irritation, sneezing and dry cough are only encountered during the
work shift and disappear with job change. Exposure at a
concentration near 40µg/m3 for a few hours would be
sufficient to cause these effects.

It has been demonstrated that an
exposure mainly above 50µg/m3 causes an increase in the
prevalence of exertional shortness of breath in a refinery where
workers were exposed to metallic cobalt, oxides and salts.

b-Spasmodic Rhinitis or Occupational
Asthma :

The clinical picture may be one of
spasmodic rhinitis or typical, true, classical occupational asthma
with a probable immunologic origin. Antibodies (IgE) against the
cobalt-albumin complex have been found in the serum of patients
suffering from cobalt asthma.

A cobalt chloride challenge test may be
positive.

In the hard metal industry, cobalt
asthma may occur at levels of exposure lower than
50µg/m3.

In one report, the syndrome did not
develop until after 6 to 18 months of exposure.

There is no evidence that this type of
disease progresses to interstitial fibrosis.

c-Allergic Alveolitis :

Symptoms may ressemble those of allergic
alveolitis (shortness of breath, chills, fever).

Cases have been described among workers
exposed to cobalt in cutting oils used to polish hard metals.
Symptoms disappear when workers are away from work for 1 month
but, come back when work resumes. The alveolitis may be associated
with a bronchoconstrictive reaction.

On clinical grounds, functionnal and
radiologic, this syndrome in its acute phase resembles the
previous one and we may ask ourselves if a distinction between the
two syndromes is justified.

At the beginning of the disease,
symptomatogy may be very scarce (dry cough, exertional shortness
of breath) and the chest X-ray may seem normal. If exposure
persists, general health state may deteriorate and a rapidly fatal
alveolitis may occur.

This disease has been observed mainly in
hard metal and diamond industries.

Cobalt may cause allergic dermatitis
with positive skin patch tests( urticaria and/or exzema). Cobalt
itself is a sensitizer as well as different salts and oxides.

This allergic dermatitis of an
erythematous papular type usually occurs in the skin areas
subjected to friction, such as the ankle, elbow flexures, and
sides of the neck.

Even if there is no cross allergy
between metals, sensitization to cobalt is often encountered in
patients already allergic to chromium and/or nickel.

Other effects :

-Cobalt cardiomyopathy has been
described in workers exposed to cobalt in different
situations.

-Polycythemia could be encountrered
among workers exposed to cobalt in the production of fritted
metallic carbides.

-One case of progressive deafness and
optic nerve atrophy has been attributed to a severe exposure to
powdered metallic cobalt for 20 months.

-Sub-clinical hypothyroidism has been
described among workers exposed exclusively to cobalt in a
refinery of this metal.

-Ocular effects have included congestion
of conjunctiva.

Carcinogenesis
:

In man, it has been suggested that
cobalt was carcinogenic(lung cancer); it is most probable that it
is due to its association with other particles such as tungsten
carbide, or concomitant exposure to arsenic and nickel as
suggested among workers employed in cobalt recycling in nickel
extraction firms.

A significant increase in lung cancer
has been observed among workers of some hard metal industries, but
not in others.

It is agreed that human data are
insufficient to conclude that cobalt per se is carcinogenic in
man.

Cobalt has been designated as being
possibly carcinogenic to humans, group 2B, by IARC.

Taking into account data from
epidemiologic studies, it is possible that exposure to dusts from
hard metals may increase the risk of lung cancer but this requires
confirmation.

Medical Surveillance
:

Cobalt in blood and urine mainly
reflects recent exposure.

Among workers exposed to cobalt-tungsten
carbide dust, a good correlation was found between the severity of
exposure to cobalt and its concentration in urine at the end of
the work week. Taking into account the biologic half-life of
urinary cobalt, its concentration at the end of the work week
reflects mostly the average exposure of previous days. Under these
circumstances, an average exposure of 0.1 mg/m3 would lead to a
urinary concentration of 60 µg/L at the end of the work
week.

End of shift blood and urine cobalt also
eflects severity of exposure.

ACGIH proposed in 1996 :

-Urine :15 µg/ L as a biological
limit (end of work week) corresponding to an atmospheric TLV of 20
µg/m3.